From: Terry S. Singeltary Sr.
Sent: Thursday, December 24, 2015 10:06 AM
Subject: Infectious disease spread is fueled by international trade
Public Release: 22-Dec-2015 Infectious disease spread is fueled by
international trade
Arizona State University
Share Print E-Mail Tempe, Ariz., (December 22, 2015) - International trade
and travel has literally opened up new vistas for humans, ranging from travel to
exotic places to enjoying the products and services of those distant lands. But
along with international trade and travel comes the risk of spreading infectious
diseases, a growing problem in today's global economy, says an Arizona State
University researcher.
"The recent Ebola outbreak made us realize that we are all just a plane
ride away from exposure to emerging infectious diseases," says Charles Perrings,
an ASU professor of environmental economics. Perrings recently published the
paper, "Options for Managing the Infectious Animal and Plant Disease Risks of
International Trade," in the early online version of the journal Food Security.
The paper reported project results to an international conference "Global
Plant Health Risks and Consequences: Linking Science, Economics and Policy,"
hosted by the British Food and Environment Research Agency, and supported by the
Organisation for Economic Cooperation and Development's Cooperative Research
Programme on Biological Resource Management for Sustainable Agricultural
Systems. Perrings is the principle investigator of a project funded by the
National Science Foundation-National Institutes of Health-U.S. Department of
Agriculture Ecology and Evolution of Infectious Diseases program in
collaboration with the UK's Biotechnology and Biological Sciences Research
Council.
In the paper, Perrings describes the growth of international trade since
the 1950s and the increasingly tight coupling of developed and developing
economies. The paper considers how the global community currently deals with
trade-related infectious disease risks of animals and plants, and asks how the
system could be made more effective.
An example of the impact of an infectious disease came in 2001 in the UK
when an outbreak of hoof and mouth disease cost some $10 billion and more than 2
million sheep and cattle had to be destroyed, Perrings said. More recently,
African swine fever--a much more serious disease of pigs--has been spread in the
Caucasus region through trade in pork, pork product or through waste in trade
vehicles.
"The more trade grows as a proportion of global production, the more likely
it is that diseases will be spread through trade, and the higher the economic
cost of resulting trade bans," Perrings said. "What is at risk is the food we
eat, the fibers we wear and build with, and the fuels we burn."
"In addition many infectious diseases that affect animals also affect
people," he added. "Zoonoses like SARS, MERS, HIV AIDS, or highly pathogenic
avian influenza, all originated in wild animals and were then spread person to
person through trade and travel."
Perrings said current instruments to control infectious diseases are far
from adequate, as the recent report of the Harvard-London School of Hygiene and
Tropical Medicine Independent Panel on the Global Response to Ebola, published
in the Lancet, makes clear.
"There are two problems to address," he said. "One is that disease spread
is an unintended (external) effect of trade. To solve this problem exporters and
importers need to be confronted with the risks they impose on consumers."
"The other is that the control of infectious disease is a public good--the
benefits it offers are freely available to all, and so will be undersupplied if
left to the market," he explained. "To solve this problem we need to undertake
cooperative, collective control of infectious diseases at the source."
Perrings said options for solving both problems include the use of payments
for risk reduction in developing countries and the development of a global fund
for infectious disease control.
At the moment countries have the right (through the Sanitary and
Phytosanitary Agreement) to act in their own defense once a disease has been
introduced. Their options are to control the outbreak and to reduce the chance
of reinfection by banning trade with risky countries or in risky products. But
this cannot stop the emergence of new diseases.
"The One Health Initiative suggests that what is needed is cooperative
collective action to reduce risk at the source," Perrings said. "This requires a
partnership between the rich countries that have the resources to fund global
prevention, and the poor countries where disease is most likely to
emerge."
"The management of infectious diseases of animals and plants, like the
management of infectious diseases of people, is now a global problem that
requires global solutions," Perrings writes. "This in turn requires a more
strongly coordinated and cooperative approach than is currently allowed under
the General Agreement on Tariffs and Trade (GATT) and the Sanitary and
Phytosanitary Agreement."
###
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Greetings AAAS et al @ EurekAlert,
I kindly wish to comment, and submit the following to you please.
>>> "There are two problems to address," he said. "One is that
disease spread is an unintended (external) effect of trade. To solve this
problem exporters and importers need to be confronted with the risks they impose
on consumers." <<<
just call it what it is, the legal trading of all strains of mad cow
disease Bovine Spongiform Encephalopathy BSE Transmissible Spongiform
Encephalopathy TSE Prion disease, spread by the OIE USDA BSE Minimal Risk Region
MRR policy.
like it or not, consumers human life are expendable now due to the BSE MRR
policy. it’s as simple as that. sound science does not matter anymore, it’s all
about trade, and nothing else matters. it is a proven fact with the BSE MRR
instead of the BSE GBR’s. ...it’s all about money now folks $$$
Saturday, December 12, 2015
CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
Thursday, December 17, 2015
Annual report of the Scientific Network on BSE-TSE 2015 EFSA-Q-2015-00738
10 December 2015
Saturday, December 12, 2015
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
Saturday, December 12, 2015
NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE
Prion REPORT December 14, 2015
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary:
The transmissible spongiform encephalopathies (also called prion diseases)
are fatal neurodegenerative diseases that affect animals and humans. The agent
of prion diseases is a misfolded form of the prion protein that is resistant to
breakdown by the host cells. Since all mammals express prion protein on the
surface of various cells such as neurons, all mammals are, in theory, capable of
replicating prion diseases. One example of a prion disease, bovine spongiform
encephalopathy (BSE; also called mad cow disease), has been shown to infect
cattle, sheep, exotic undulates, cats, non-human primates, and humans when the
new host is exposed to feeds or foods contaminated with the disease agent. The
purpose of this study was to test whether non-human primates (cynomologous
macaque) are susceptible to the agent of sheep scrapie. After an incubation
period of approximately 10 years a macaque developed progressive clinical signs
suggestive of neurologic disease. Upon postmortem examination and microscopic
examination of tissues, there was a widespread distribution of lesions
consistent with a transmissible spongiform encephalopathy. This information will
have a scientific impact since it is the first study that demonstrates the
transmission of scrapie to a non-human primate with a close genetic relationship
to humans. This information is especially useful to regulatory officials and
those involved with risk assessment of the potential transmission of animal
prion diseases to humans.
Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion
disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the
past decades, c-BSE's zoonotic potential has been the driving force in
establishing extensive protective measures for animal and human health. In
complement to the recent demonstration that humanized mice are susceptible to
scrapie, we report here the first observation of direct transmission of a
natural classical scrapie isolate to a macaque after a 10-year incubation
period. Neuropathologic examination revealed all of the features of a prion
disease: spongiform change, neuronal loss, and accumulation of PrPres throughout
the CNS.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats
SUMMARY: We are reopening the comment period for our proposed rule that
would revise completely the scrapie regulations, which concern the risk groups
and categories established for individual animals and for flocks, the use of
genetic testing as a means of assigning risk levels to animals, movement
restrictions for animals found to be genetically less susceptible or resistant
to scrapie, and recordkeeping requirements. This action will allow interested
persons additional time to prepare and submit comments.
DATES: The comment period for the proposed rule published on September 10,
2015 (80 FR 54660-54692) is reopened. We will consider all comments that we
receive on or before December 9, 2015. ...
COMMENT SUBMISSION TERRY S. SINGELTARY SR.
WITH regards to Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats, I
kindly submit the following ;
>>>The last major revision of the scrapie regulations occurred on
August 21, 2001, when we published in theFederal Register(66 FR 43964, Docket
No. 97-093-5) a final rule amending part 79 by imposing additional restrictions
on the interstate movement of sheep and goats.<<<
Indeed, much science has changed about the Scrapie TSE prion, including
more science linking Scrapie to humans. sadly, politics, industry, and trade,
have not changed, and those usually trump sound science, as is the case with all
Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing
animals and the OIE. we can look no further at the legal trading of the Scrapie
TSE prion both typical and atypical of all strains, and CWD all stains. With as
much science of old, and now more new science to back this up, Scrapie of all
types i.e. atypical and typical, BSE all strains, and CWD all strains, should be
regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE,
and all trading partners to take heed to the latest science on the TSE prion
disease, all of them, and seriously reconsider the blatant disregards for human
and animal health, all in the name of trade, with the continued relaxing of TSE
Prion trade regulations through the ‘NEGLIGIBLE BSE RISK’ PROGRAM, which was set
up to fail in the first place. If the world does not go back to the ‘BSE RISK
ASSESSMENTS’, enhance, and or change that assessment process to include all TSE
prion disease, i.e. ‘TSE RISK ASSESSMENT’, if we do not do this and if we
continue this farce with OIE and the USDA et al, and the ‘NEGLIGIBLE BSE RISK’
PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they
will continue to mutate and spread among species of human and animal origin, and
they will continue to kill. ...
please see ;
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Evaluation of the zoonotic potential of transmissible mink
encephalopathy
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Ruchoux,
Marie-Madeleine - item Durand, Valerie - item Luccantoni-Freire, Sophie - item
Dehen, Capucine - item Correia, Evelyne - item Casalone, Cristina - item Richt,
Juergen item Greenlee, Justin item Torres, Juan Maria - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Pathogens Publication Type: Peer Reviewed Journal Publication
Acceptance Date: July 30, 2013 Publication Date: July 30, 2013 Citation: Comoy,
E.E., Mikol, J., Ruchoux, M., Durand, V., Luccantoni-Freire, S., Dehen, C.,
Correia, E., Casalone, C., Richt, J.A., Greenlee, J.J., Torres, J.M., Brown, P.,
Deslys, J. 2013. Evaluation of the zoonotic potential of transmissible mink
encephalopathy. Pathogens. 2:(3)520-532.
Interpretive Summary: Cases of bovine spongiform encephalopathy (BSE) or
mad cow disease can be subclassified into at least 3 distinct disease forms with
the predominate form known as classical BSE and the others collectively referred
to as atypical BSE. Atypical BSE can be further subdivided into H-type and
L-type cases that are distinct from classical BSE and from each other. Both of
the atypical BSE subtypes are believed to occur spontaneously, whereas classical
BSE is spread through feeding contaminated meat and bone meal to cattle.
Transmissible mink encephalopathy (TME) is another prion disease that transmits
to cattle and show similarities to L-type BSE when subjected to laboratory
testing. The purpose of this study was to use non-human primates (cynomologous
macaque) and transgenic mice expressing the human prion protein to determine if
TME could represent a potential risk to human health. TME from two sources
(cattle and raccoons) was able to infect non-human primates and transgenic mice
after exposure by the intracranial route. This result suggest that humans may be
able to replicate TME prions after an exposure that allows infectious material
access to brain tissue. At this time, it is unknown whether non-human primates
or transgenic mice would be susceptible to TME prions after oral exposure. The
results obtained in these animal models were similar to those obtained for
L-type BSE. Although rare, the existence of TME and that it transmits to cattle,
non-human primates, and transgenic mice suggest that feed bans preventing the
feeding of mammalian tissues to cattle should stay in place and that regular
prion surveillance during the slaughter should remain in place. Parties with
interest in the cattle and beef industries and regulatory officials responsible
for safe feeding practices of cattle will be interested in this work. Technical
Abstract: Successful transmission of Transmissible Mink Encephalopathy (TME) to
cattle supports the bovine hypothesis to the still controversial origin of TME
outbreaks. Human and primate susceptibility to classical Bovine Spongiform
Encephalopathy (c-BSE) and the transmissibility of L-type BSE to macaques assume
a low cattle-to-primate species barrier: we therefore evaluated the zoonotic
potential of cattle-adapted TME. In less than two years, this strain induced in
cynomolgus macaques a neurological disease similar to L-BSE and distinct from
c-BSE. TME derived from another donor species (raccoon) induced a similar
disease with shorter incubation periods.
*** L-BSE and cattle-adapted TME were also transmissible to transgenic mice
expressing human PrP. Interestingly, secondary transmissions to transgenic mice
expressing bovine PrP showed the maintenance of prion strain features for the
three tested bovine prion strains (cattle TME, c-BSE and L-BSE) regardless of
intermediate host.
*** Thus, TME is the third animal prion strain transmissible to both
macaques and humanized transgenic mice, suggesting zoonotic potentials that
should be considered in the risk analysis of animal prion diseases for human
health.
*** Moreover, the similarities between TME and L-BSE are highly suggestive
of a link between those strains, and of the presence of L-BSE decades prior to
its identification in USA and Europe.
Research Project: Transmission, Differentiation, and Pathobiology of
Transmissible Spongiform Encephalopathies
2014 Annual Report
1a.Objectives (from AD-416): 1. Investigate the pathobiology of atypical
transmissible spongiform encephalopathies (TSEs) in natural hosts. A.
Investigate the pathobiology of atypical scrapie. B. Investigate the
pathobiology of atypical bovine spongiform encephalopathy (BSE). 2. Investigate
the horizontal transmission of TSEs. A. Assess the horizontal transmission of
sheep scrapie in the absence of lambing. B. Determine routes of transmission in
chronic wasting disease (CWD) infected premises. C. Assess oral transmission of
CWD in reindeer. 3. Investigate determinants of CWD persistence. A. Determine
CWD host range using natural routes of transmission. B. Investigate the
pathobiology of CWD.
1b.Approach (from AD-416): The studies will focus on three animal
transmissible spongiform encephalopathy (TSE) agents found in the United States:
bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic
wasting disease (CWD) of deer, elk, and moose. The research will address sites
of accumulation, routes of infection, environmental persistence, and ante mortem
diagnostics with an emphasis on controlled conditions and natural routes of
infection. Techniques used will include clinical exams, histopathology,
immunohistochemistry and biochemical analysis of proteins. The enhanced
knowledge gained from this work will help mitigate the potential for
unrecognized epidemic expansions of these diseases in populations of animals
that could either directly or indirectly affect food animals.
3.Progress Report: Research efforts directed toward meeting objective 1 of
our project plan, Investigate the pathobiology of atypical transmissible
spongiform encephalopathies (TSEs) in natural hosts, include work in previous
years starting with the inoculation of animals for studies designed to address
the pathobiology of atypical scrapie, atypical bovine spongiform encephalopathy
(BSE), as well as a genetic version of BSE. Animals inoculated with atypical
scrapie have not yet developed disease. Atypical BSE animals have developed
disease and evaluation of the samples is currently underway. Animals inoculated
with a genetic version of BSE have developed disease and the manuscript has been
published (2012). In addition, we have investigated the possibility that
atypical scrapie was present earlier than previously detected in the national
flock by analyzing archived field isolates using methods that were unavailable
at the time of original diagnosis. Sample quality was sufficiently degraded that
modern methods were not suitable for evaluation. In research pertaining to
objective 2, Investigate the horizontal transmission of TSEs, we have initiated
a study to determine if cohousing non-lambing scrapie inoculated sheep is
sufficient to transmit scrapie to neonatal lambs. At this time, scrapie free
ewes have lambed in the presence of scrapie inoculated animals and the lambs are
cohoused with these inoculated animals.
4.Accomplishments 1. Evaluated enzyme immunoassay for rapid identification
of prion disease in livestock. Scrapie of sheep and bovine spongiform
encephalopathy of cattle are diseases that cause damage to the central nervous
system including the retina in the eye. The infectious agent is an abnormal
protein called a prion that has misfolded from its normal state and is resistant
to breakdown by the host cells. Current diagnostic methods require the testing
of brain material, which can be difficult to collect and may lead to
contamination of the environment and exposure of personnel to the infectious
agent. Eyes can be readily collected without opening the skull. ARS researchers
at Ames, Iowa demonstrated that the enzyme immunoassay results using eyes of
negative controls or samples collected from sheep or cattle with clinical signs
were in agreement with approved confirmatory assays (western blot or
immunohistochemistry). These results indicate the retina is a useful tissue for
rapid diagnosis of prion disease in clinically ill sheep and cattle and could be
considered to greatly increase the number of samples submitted for prion disease
diagnosis with a minimal investment of time and limited exposure of personnel to
prion agents.
2. Evaluated E211K cattle as a model for inherited human prion disease.
Prion diseases cause damage to the central nervous system of animals and humans.
The infectious agent is an abnormal protein called a prion that has misfolded
from its normal state and is resistant to breakdown by the host cells and thus
accumulates and damages those cells. Some forms of prion disease are genetic and
can be inherited. Current models of genetic prion disease in humans rely on
mouse models expressing either the human prion protein (E200K) or a combination
of both mouse and human sequences. In addition to being an entirely artificial
system these mouse models have a short lifespan making them a less than ideal
system to study a naturally occurring genetic disorder with a long incubation
time and late onset of disease. Cattle, however, exhibit a number of
similarities to humans with regard to prion disease and perhaps most notable is
the late onset of genetic prion disease. ARS researchers at Ames, Iowa have
produced cattle containing both 1 and 2 chromosome copies of the cattle prion
gene (E211K) and evaluated many aspects of this prion protein from cattle
including protein stability, protein expression levels and ratios, as well as
evidence of oxidative stress. Taken together, these results highlight the
differences between mouse models of genetic prion disease and a naturally
occurring prion disease system in cattle and suggest that cattle will provide a
more relevant understanding of genetic prion disease in humans than do current
rodent models.
Review Publications Smith, J.D., Greenlee, J.J. 2014. Detection of
misfolded prion protein in retina samples of sheep and cattle by use of a
commercially available enzyme immunoassay. American Journal of Veterinary
Research. 75(3):268-272. Haldar, S., Beveridge, A.J., Wong, J., Singh, A.J.,
Galimberti, D., Borroni, D., Zhu, X., Blevins, J., Greenlee, J., Perry, G.,
Mukhopadhyay, C.K., Schmotzer, C., Singh, N. 2014. A low-molecular-weight
ferroxidase is increased in the CSF of sCJD Cases: CSF ferroxidase and
transferrin as diagnostic biomarkers for sCJD. Antioxidants & Redox
Signaling. 19(14):1662-1675.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=421870&fy=2014
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=421870
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease
Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of the agent of sheep scrapie to deer results in PrPSc
with two distinct molecular profiles Authors
item Greenlee, Justin item Moore, Sarah - item Smith, Jodi item West
Greenlee, Mary - item Kunkle, Robert
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance
Date: March 31, 2015 Publication Date: May 25, 2015 Citation: Greenlee, J.,
Moore, S.J., Smith, J.., West Greenlee, M.H., Kunkle, R. 2015.
Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum. Prion 2015. p. S62. Technical Abstract: The purpose of this
work was to determine susceptibility of white-tailed deer (WTD) to the agent of
sheep scrapie and to compare the resultant PrPSc to that of the original
inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route
of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie
isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc
was detected in lymphoid tissues at preclinical time points, and deer necropsied
after 28 months post-inoculation had clinical signs, spongiform encephalopathy,
and widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes reveal PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile type readily passes to deer.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A
Technical Abstract: The purpose of this work was to determine
susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to
compare the resultant PrPSc to that of the original inoculum and chronic wasting
disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral
and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer
had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at
preclinical time points, and deer necropsied after 28 months post-inoculation
had clinical signs, spongiform encephalopathy, and widespread distribution of
PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with
2 distinct molecular profiles. WB on cerebral cortex had a profile similar to
the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph
nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the
2 distinct profiles from WTD with clinical scrapie were further passaged to mice
expressing cervid prion protein and intranasally to sheep and WTD. In cervidized
mice, the two inocula have distinct incubation times. Sheep inoculated
intranasally with WTD derived scrapie developed disease, but only after
inoculation with the inoculum that had a scrapie-like profile. The WTD study is
ongoing, but deer in both inoculation groups are positive for PrPSc by rectal
mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to
the agent of scrapie, two distinct molecular profiles of PrPSc are present in
the tissues of affected deer, and inoculum of either profile readily passes to
deer.
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
==========================================
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==========================================
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
***********OCTOBER 2015*************
*** PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS ***
THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and
Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and
Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.
P.108: Successful oral challenge of adult cattle with classical BSE
Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine
Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge;
Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology
Laboratory; Truro, Nova Scotia, Canada
Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and
food-borne fatal neurological disease which can be orally transmitted to cattle
and humans. Due to the presence of contaminated milk replacer, it is generally
assumed that cattle become infected early in life as calves and then succumb to
disease as adults. Here we challenged three 14 months old cattle per-orally with
100 grams of C-type BSE brain to investigate age-related susceptibility or
resistance. During incubation, the animals were sampled monthly for blood and
feces and subjected to standardized testing to identify changes related to
neurological disease. At 53 months post exposure, progressive signs of central
nervous system disease were observed in these 3 animals, and they were
euthanized. Two of the C-BSE animals tested strongly positive using standard BSE
rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts
S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing
resulted in the detection of pathologic lesion in unusual brain location and
PrPsc detection by PMCA only. Our study demonstrates susceptibility of adult
cattle to oral transmission of classical BSE. We are further examining
explanations for the unusual disease presentation in the third challenged
animal.
***Our study demonstrates susceptibility of adult cattle to oral
transmission of classical BSE. ***
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. ***
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants
and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and
humans at the molecular level, we investigated the ability of abnormal prion
protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical
scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to
proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding
cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from
transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc
seed from typical and atypical BSE- or typical scrapie-infected brain
homogenates from native host species. In the conventional PMCA, the conversion
of PrPC to PrPres was observed only when the species of PrPC source and PrPSc
seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA
and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested
prion strains. On the other hand, human PrPC was converted by PrPSc from typical
and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports
describing the lack of transmissibility of H-type BSE to ovine and human
transgenic mice, ***our findings suggest that possible transmission risk of
H-type BSE to sheep and human. Bioassay will be required to determine whether
the PMCA products are infectious to these animals.
================
==========================================
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==========================================
Thursday, December 17, 2015
Annual report of the Scientific Network on BSE-TSE 2015 EFSA-Q-2015-00738
10 December 2015
Saturday, December 12, 2015
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
Saturday, December 12, 2015
NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE
Prion REPORT December 14, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...see more here ;
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Tuesday, December 15, 2015
Chronic Wasting Disease will cause a Wyoming deer herd to go virtually
extinct in 41 years, a five-year study predicts
Study: Chronic Wasting Disease kills 19% of deer herd annually
Chronic Wasting Disease will cause a Wyoming deer herd to go virtually
extinct in 41 years, a five-year study predicts.
The investigation, which relied on the capture of 143 deer, examined the
dynamics in the Southern Converse County Mule Deer Herd that lives southwest of
Douglas near Laramie Peak. There, a population that once numbered some 14,000 in
the early 2000s dwindled to half that size in about a decade.
The Chronic Wasting Disease study is one of only three that have been
conducted on wild deer, elk or moose herds, none of which have yet seen print.
While wildlife managers have long suspected CWD as a principle agent in the
ravaged Converse herd, the study puts numbers on the problem, calculating a 19
percent decline annually.
University of Wyoming doctoral student Melia DeVivo spent four years of
fieldwork and another year crunching numbers before defending her PhD thesis on
the herd. She calculated the herd would go extinct in 41 years, without taking
into account genetic differences that make some deer more resistant to CWD, or
accounting for deer migration into the area. Even when taking in those factors,
the herd will decline dramatically, she said.
“I estimated that CWD was causing a 19 percent annual reduction in the
population, which is pretty significant,” she said. “Potentially, in 41 years,
it would be locally extinct.”
snip...see full text ;
Saturday, December 05, 2015
CWD Prions Remain Infectious after Passage Through the Digestive System of
Coyotes (Canis latrans)
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26
April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated
online 11 September 2015 Erratum (October, 2015)
*** Evidence for human transmission of amyloid-β pathology and cerebral
amyloid angiopathy
07 02:27 AM
re-Evidence for human transmission of amyloid-? pathology and cerebral
amyloid angiopathy
*** Terry S. Singeltary Sr. said:
I would kindly like to comment on the Nature Paper, the Lancet reply, and
the newspaper articles.
snip...see full text ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO
PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
snip...
4. The other dimension to consider is the public reaction. To some extent
the GSS case demonstrates little more than the transmission of BSE to a pig by
intra-cerebral injection. If other prion diseases can be transmitted in this way
it is little surprise that some pathological findings observed in GSS were also
transmissible to a marmoset. But the transmission of features of Alzheimer's
pathology is a different matter, given the much greater frequency of this
disease and raises the unanswered question whether some cases are the result of
a transmissible prion. The only tenable public line will be that "more research
is required’’ before that hypothesis could be evaluated. The possibility on a
transmissible prion remains open. In the meantime MRC needs carefully to
consider the range and sequence of studies needed to follow through from the
preliminary observations in these two cases. Not a particularly comfortable
message, but until we know more about the causation of Alzheimer's disease the
total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH
832 llllYc!eS 2 92/11.4/1.2
>>> The only tenable public line will be that "more research is
required’’ <<<
>>> possibility on a transmissible prion remains
open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is
"more research is required’’ enough time for evaluation ?
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Merry Christmas !
kindest regards, terry
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
